Abstract
Highlights| February 01 2023 Selected Articles from This Issue Author & Article Information Online Issn: 1557-3125 Print Issn: 1541-7786 ©2023 American Association for Cancer Research2023American Association for Cancer Research Mol Cancer Res (2023) 21 (2): 89. https://doi.org/10.1158/1541-7786.MCR-21-2-HI Related Content A commentary has been published: BET Inhibitors Target the SCLC-N Subtype of Small-Cell Lung Cancer by Blocking NEUROD1 Transactivation A commentary has been published: Downregulation of iNOS/NO Promotes Epithelial–Mesenchymal Transition and Metastasis in Colorectal Cancer A commentary has been published: TWEAK–Fn14–RelB Signaling Cascade Promotes Stem Cell–like Features that Contribute to Post-Chemotherapy Ovarian Cancer Relapse View more A commentary has been published: XIAP and PHB1 Regulate Anoikis through Competitive Binding to TRAF6 View less Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record February 1 2023 Citation Selected Articles from This Issue. Mol Cancer Res 1 February 2023; 21 (2): 89. https://doi.org/10.1158/1541-7786.MCR-21-2-HI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search NEUROD1 is the master transcriptional regulator defining the small-cell lung cancer (SCLC) SCLC-N subtype, but NEUROD1 has proven difficult to therapeutically target. Targeting NEUROD1 transcriptional coactivators may be an effective therapeutic approach, but such coactivators have yet to be defined. To identify NEUROD1 transcriptional coactivators, Chen and colleagues elucidated NEUROD1 genomic localization regions using ChIP-Seq and searched for colocalizing coactivator candidates using a ChIP-Seq database. The authors discovered that BRD4, a member of the bromodomain and extraterminal domain (BET) protein family, significantly colocalizes to NEUROD1-inhabited genomic regions. Co-immunoprecipitation experiments demonstrated that BRD4 and NEUROD1 interact, and treatment with BET inhibitors (BETi) decreases NEUROD1 target gene expression, suggesting BRD4 is a NEUROD1 transcriptional coactivator. Accordingly, the authors found that SCLC-N cells are more sensitive to BETi than are other SCLC subtype cells, and that BETi significantly slow SCLC-N patient-derived xenograft tumor growth in mouse models. Using a siRNA screen, the authors... You do not currently have access to this content.
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